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Asthma: an inflammatory mediator soup.

https://arctichealth.org/en/permalink/ahliterature15650
Source
Allergy. 1999;54 Suppl 49:55-61
Publication Type
Article
Date
1999
Author
U S Björnsdottir
D M Cypcar
Author Affiliation
Pulmonary Department, University Hospital of Iceland, Vifilstadir.
Source
Allergy. 1999;54 Suppl 49:55-61
Date
1999
Language
English
Publication Type
Article
Keywords
Asthma - immunology - pathology - physiopathology
Cell Adhesion Molecules - metabolism
Cell Movement
Cytokines - metabolism
Eosinophils - physiology
Epithelial Cells - physiology
Humans
Inflammation Mediators - metabolism
T-Lymphocytes, Helper-Inducer - physiology
Abstract
Reversible or partially reversible airway obstruction, inflammation, and bronchial hyperresponsiveness to various stimuli are the defining characteristics of asthma. Airway obstruction in asthma is a complex event that is due to bronchospasm, inflammation, and mucus formation. Inflammation has assumed a more central role in the pathogenesis of the disease, as it contributes not only to airflow obstruction, but also to bronchial hyperresponsiveness. The inciting trigger, or inhaled allergen, in asthma induces the activation of mast cells and macrophages with the subsequent release of several proinflammatory mediators, including leukotrienes, chemotactic factors, and cytokines. Antigen processed by macrophages is presented to undifferentiated T helper cells, inducing differentiation to the Th2 phenotype, with the subsequent release of IL-4 and IL-5, causing IgE synthesis and eosinophil infiltration, respectively. Macrophage-derived cytokines, such as IL-1, TNF-alpha, and IFN-gamma, activate endothelial cells, upregulating the expression of adhesion molecules such as ICAM-1 and VCAM-1, which permit egression of leukocytes from the vasculature to the airway mucosa. Several inflammatory cells, such as eosinophils, mast cells, and macrophages, not only cause airway damage, but also synthesize cytokines that perpetuate the inflammatory process. This complex interplay of inflammatory cells and mediators causes the classic histopathophysiologic features in the airways of both symptomatic and asymptomatic individuals with asthma, emphasizing the importance of early recognition and antiinflammatory treatment.
PubMed ID
10422749 View in PubMed
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The effect of immunotherapy on bronchial hyperresponsiveness and eosinophil cationic protein in pollen-allergic patients.

https://arctichealth.org/en/permalink/ahliterature16167
Source
J Allergy Clin Immunol. 1988 Sep;82(3 Pt 1):470-80
Publication Type
Article
Date
Sep-1988
Author
S. Rak
O. Löwhagen
P. Venge
Author Affiliation
Department of Lung Medicine, Central Hospital, Västerås, Gothenburg.
Source
J Allergy Clin Immunol. 1988 Sep;82(3 Pt 1):470-80
Date
Sep-1988
Language
English
Publication Type
Article
Keywords
Allergens
Asthma - therapy
Blood Proteins - physiology
Bronchi - physiopathology
Bronchial Provocation Tests
Eosinophil Granule Proteins
Eosinophils - physiology
Forced expiratory volume
Immunotherapy
Nasal Provocation Tests
Pollen - immunology
Rhinitis, Allergic, Seasonal - therapy
Ribonucleases
Seasons
Skin Tests
Trees
Abstract
The effect of immunotherapy (IT) on bronchial response to histamine and on eosinophil cationic protein (ECP) in 40 birch pollen-allergic patients with a history of rhinoconjunctivitis and wheezing during the birch season was examined. Twenty patients started IT with birch extract (Pharmacia, Uppsala, Sweden) before the season. The other 20 patients were not treated with IT. Histamine-challenge tests were performed before, at the start, at pollen peak, at the end, and after the birch-pollen season. Blood samples for determination of ECP were collected at the same time. Skin prick tests and nasal provocation tests were also performed before and after the season. A significant increase in bronchial hyperresponsiveness was noted in the group treated with IT and in the untreated group during the season. The increase was greatest in the untreated group with the maximal difference between the two groups at the end of the pollen season (p less than 0.07). IT treatment was followed by significantly less medication and higher peak expiratory flow values. The levels of ECP increased during the season in untreated patients (p less than 0.05) but not in patients treated with IT. The ECP levels of patients from both groups correlated significantly with histamine sensitivity (p less than 0.001).
PubMed ID
3170995 View in PubMed
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Eosinophil inflammation of nasal polyp tissue: relationships with matrix metalloproteinases, tissue inhibitor of metalloproteinase-1, and transforming growth factor-beta1.

https://arctichealth.org/en/permalink/ahliterature15287
Source
J Korean Med Sci. 2003 Feb;18(1):97-102
Publication Type
Article
Date
Feb-2003
Author
Young-Mok Lee
Sun-Sin Kim
Hyun-Ah Kim
Yu-Jin Suh
Soo-Keol Lee
Dong-Ho Nahm
Hae-Sim Park
Author Affiliation
Department of Allergy and Clinical Immunology, Ajou University School of Medicine, Suwon, Korea. hspark@madang.ajou.ac.kr
Source
J Korean Med Sci. 2003 Feb;18(1):97-102
Date
Feb-2003
Language
English
Publication Type
Article
Keywords
Adult
Asthma - complications
Blood Proteins - analysis
Chemotaxis, Leukocyte
Eosinophil Granule Proteins
Eosinophilia - etiology - metabolism - pathology
Eosinophils - physiology
Female
Gelatinase A - analysis - physiology
Gelatinase B - analysis - physiology
Humans
Male
Mast Cells - physiology
Middle Aged
Nasal Polyps - chemistry - etiology - pathology
Rhinitis - metabolism - pathology
Ribonucleases
Serine Endopeptidases - analysis
Tissue Inhibitor of Metalloproteinase-1 - analysis - physiology
Transforming Growth Factor beta - analysis - physiology
Abstract
Eosinophil and mast cell infiltrations are consistent findings in nasal polyp tissue. Previous studies have shown that matrix metalloproteinases (MMPs) may be involved in eosinophil infiltration in airway mucosa of asthmatic patients, and that transforming growth factor-beta1 (TGF-beta1) induces extracellular matrix deposition in nasal polyp tissue. The aim of this study was to evaluate the role of MMPs and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in association with TGF-beta1, eosinophils and mast cell activation in nasal polyp tissue. Nasal polyp tissues from 20 patients who underwent polypectomies were collected and prepared into tissue homogenate. Eosinophil cationic protein (ECP) and tryptase levels were measured by CAP system (Pharmacia, Sweden). MMP-2, MMP-9, TIMP-1 and TGF-beta1 levels were measured by enzyme-liked immunosorbent assay. MMP-2 was the predominant form of MMPs, followed by MMP-9 and TIMP-1. There were significant correlations between ECP, and MMP-9, MMP-2, TGF-beta1 and tryptase, but not with TIMP-1. Significant correlations were noted between tryptase, and MMP-2, MMP-9, and TGF-beta1, but not with TIMP-1. Close correlations were noted between TGF-beta1, and MMP-9 and MMP-2, but not with TIMP-1. MMP-2, MMP-9, and TGF-beta1 may contribute to eosinophil and mast cell migrations into nasal polyp tissue.
PubMed ID
12589095 View in PubMed
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Interleukin-4-mediated infiltration of eosinophils into the conjunctiva and its suppression by interferon-gamma.

https://arctichealth.org/en/permalink/ahliterature50578
Source
Curr Eye Res. 2005 Feb;30(2):115-22
Publication Type
Article
Date
Feb-2005
Author
Atsuki Fukushima
Zhang Jian
Waka Ishida
Kazuyo Fukata
Akemi Ozaki
Hisayuki Ueno
Author Affiliation
Department of Ophthalmology, Kochi Medical School, Kohasu, Nankoku-city, Japan. fukusima@med.kochi-u.ac.jp
Source
Curr Eye Res. 2005 Feb;30(2):115-22
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Animals
Cell Count
Cell Movement - drug effects
Chemokines - metabolism
Chemokines, CC - pharmacology
Conjunctiva - cytology - metabolism
Cytokines - metabolism
Dose-Response Relationship, Drug
Drug Combinations
Eosinophils - physiology
Injections
Interferon-gamma, Recombinant - pharmacology
Interleukin-4 - pharmacology
Male
Rats
Rats, Inbred BN
Recombinant Proteins
Reverse Transcriptase Polymerase Chain Reaction
Up-Regulation
Abstract
PURPOSE: Interleukin (IL)-4 is a T helper (Th)2 cytokine that plays an important role in the development of allergic reactions. It has been suggested that IL-4 is responsible for the infiltration of eosinophils into the conjunctiva during the development of allergic conjunctivitis. However, it is still unclear whether IL-4 is able to induce this eosinophilic infiltration on its own. We investigated whether subconjunctival injection of IL-4 can induce eosinophils to infiltrate into the conjunctiva. METHODS: Brown Norway rats were subconjunctivally injected with IL-4, eotaxin, or phosphate buffered saline (PBS), and the conjunctivas were harvested for histologic analysis (including immunohistochemistry) 6, 12, 18, and 24 hr later. The harvested conjunctivas were also subjected to reverse transcription-polymerase chain reaction (RT-PCR) analysis to examine chemokine expression. In a separate experiment, the effect of coadministering interferon-gamma (IFN-gamma) along with IL-4 was examined. RESULTS: The subconjunctival injection of IL-4 induced eosinophil infiltration into the conjunctiva in a dose-dependent manner. IL-4 was as potent as eotaxin. The eosinophilic infiltration started 6 hr after the injection and persisted for up to 24 hr after the injection. Other infiltrating cell phenotypes were noted but were also observed in conjunctivas injected with PBS alone. RT-PCR analysis demonstrated that IL-4 injection did not upregulate chemokine RNA expression in the conjunctiva. Coinjection of IFN-gamma suppressed the infiltration of eosinophils into the conjunctiva induced by IL-4 injection. CONCLUSIONS: The subconjunctival injection of IL-4 specifically induces eosinophils to infiltrate into the conjunctiva. In addition, IFN-gamma in the conjunctiva can counteract this effect of IL-4.
PubMed ID
15814469 View in PubMed
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Involvement of cysteinyl leukotrienes in airway smooth muscle cell DNA synthesis after repeated allergen exposure in sensitized Brown Norway rats.

https://arctichealth.org/en/permalink/ahliterature15646
Source
Br J Pharmacol. 1999 Jul;127(5):1151-8
Publication Type
Article
Date
Jul-1999
Author
M. Salmon
D A Walsh
T J Huang
P J Barnes
T B Leonard
D W Hay
K F Chung
Author Affiliation
Thoracic Medicine, Imperial College School of Medicine at the National Heart and Lung Institute, London, UK.
Source
Br J Pharmacol. 1999 Jul;127(5):1151-8
Date
Jul-1999
Language
English
Publication Type
Article
Keywords
Acetylcholine - pharmacology
Allergens - immunology
Animals
Arachidonate 5-Lipoxygenase - physiology
Bronchi - drug effects - metabolism
Cell Count
Cysteine - physiology
DNA - biosynthesis
Eosinophils - physiology
Leukotrienes - physiology
Male
Muscle, Smooth - metabolism
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Abstract
Airway smooth muscle thickening is a characteristic feature of airway wall remodelling in chronic asthma. We have investigated the role of the leukotrienes in airway smooth muscle (ASM) and epithelial cell DNA synthesis and ASM thickening following repeated allergen exposure in Brown Norway rats sensitized to ovalbumin. There was a 3 fold increase in ASM cell DNA synthesis, as measured by percentage bromodeoxyuridine (BrdU) incorporation, in repeatedly ovalbumin-exposed (4.1%, 3.6-4.6; mean, 95% c.i.) compared to chronically saline-exposed rats (1.3%, 0.6-2.1; P
PubMed ID
10455261 View in PubMed
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[Local eosinophilia of the nose, the larynx and the trachea in rats sensitized with Japanese cedar pollen]

https://arctichealth.org/en/permalink/ahliterature57585
Source
Arerugi. 1997 Dec;46(12):1251-7
Publication Type
Article
Date
Dec-1997
Author
J. Ishii
T. Ogawa
K. Naito
S. Miyata
M. Ishihara
R. Baba
Y. Senoh
S. Iwata
N. Yokoyama
Author Affiliation
Nagoya City Public Health Research Institute.
Source
Arerugi. 1997 Dec;46(12):1251-7
Date
Dec-1997
Language
Japanese
Publication Type
Article
Keywords
Animals
English Abstract
Eosinophils - physiology
Immunization
Laryngeal Mucosa - cytology - immunology
Male
Mucous Membrane - cytology - immunology
Nasal Mucosa - cytology - immunology
Pollen - immunology
Rats
Rats, Inbred BN
Trachea - cytology - immunology
Trees
Abstract
Eight Brown Norway rats were immunized twice at days 0 and 13 by intraperitneal injections of 10 micrograms Cry j I, one of major allergen to Japanese cedar pollinosis, mixed with 4.5 mg aluminium hydroxide gel. Serum level of Anti-Cry j I IgE antibody was detected by the method of ELISA. Mean value of serum levels of specific IgE to Cry j I in the sensitized rats was significantly higher than that in the non-sensitized five rats (p
PubMed ID
9503685 View in PubMed
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Mast-cell activation augments the late phase reaction in experimental immune-mediated blepharoconjunctivitis.

https://arctichealth.org/en/permalink/ahliterature50704
Source
Graefes Arch Clin Exp Ophthalmol. 2003 May;241(5):394-402
Publication Type
Article
Date
May-2003
Author
Akemi Ozaki
Atsuki Fukushima
Kazuyo Fukata
Hisayuki Ueno
Author Affiliation
Laboratory of Immunology, Department of Ophthalmology, Kochi Medical School, Kohasu, Oko-cho, 783-8505 Nankoku-city, Japan.
Source
Graefes Arch Clin Exp Ophthalmol. 2003 May;241(5):394-402
Date
May-2003
Language
English
Publication Type
Article
Keywords
Animals
Blepharitis - chemically induced - immunology - pathology
Cell Movement
Conjunctivitis, Allergic - chemically induced - immunology - pathology
Enzyme-Linked Immunosorbent Assay
Eosinophilia - immunology
Eosinophils - physiology
Flow Cytometry
Hypersensitivity, Delayed - immunology - pathology
Lymphocyte Activation
Male
Mast Cells - physiology
Ovalbumin - immunology
RANTES - metabolism
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Reverse Transcriptase Polymerase Chain Reaction
T-Lymphocytes - immunology
p-Methoxy-N-methylphenethylamine
Abstract
BACKGROUND: How the early phase allergic reaction affects the late phase reaction remains unclear. We examined this issue with an experimental model of allergic conjunctivitis that permits the two reactions to be disconnected from each other. METHODS: Experimental immune-mediated blepharoconjunctivitis (EC) was initiated in Brown Norway rats by transferring ovalbumin (OVA)-specific T cells and then challenging with OVA-containing eye drops. To induce early phase reaction, a mast-cell activator, C48/80, was challenged together with or without OVA. Rats were evaluated clinically and eyes were harvested for histologic examination and for evaluation of chemokine expression by reverse-transcriptase PCR. RESULTS: The rats challenged with OVA alone developed the T-cell-mediated late phase reaction histologically, but not clinically, in the absence of early phase reaction. While rats challenged with C48/80 with or without OVA exhibited clinical signs of the early phase reaction, the clinical late phase reaction was observed only in the OVA+C48/80 group. Eosinophilic infiltration into the conjunctiva during the late phase reaction of the OVA+C48/80 group markedly exceeded that of rats challenged with either OVA or C48/80 alone. RANTES (regulated on activation, normal T-cell expressed and secreted), an eosinophil attractant, was expressed both in the OVA+C48/80 and OVA groups, while eotaxin was expressed at equivalent levels in all three groups. CONCLUSION: The mast-cell-mediated early phase reaction potentiates the T-cell-mediated late phase reaction, and RANTES is involved in eosinophilic infiltration induced by antigen-specific T cells. Other molecules induced by allergen-specific T cells activated in an as yet unknown manner by the mast cells may be responsible for the infiltration of eosinophils.
PubMed ID
12682842 View in PubMed
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[Role of eosinophils and cell adhesion molecules in the asthmatic response to allergen]

https://arctichealth.org/en/permalink/ahliterature15952
Source
Nihon Kyobu Shikkan Gakkai Zasshi. 1994 Aug;32(8):721-30
Publication Type
Article
Date
Aug-1994
Author
D. Ihaku
O. Uyama
T. Matsuyama
Author Affiliation
Fifth Department of Internal Medicine, Hyogo College of Medicine, Japan.
Source
Nihon Kyobu Shikkan Gakkai Zasshi. 1994 Aug;32(8):721-30
Date
Aug-1994
Language
Japanese
Publication Type
Article
Keywords
Airway Resistance
Animals
Antigens, CD18 - immunology
Asthma - immunology
English Abstract
Eosinophils - physiology
Guinea Pigs
Intercellular Adhesion Molecule-1 - immunology - metabolism
Leukocyte Count
Male
Ovalbumin - immunology
Rats
Rats, Inbred BN
Abstract
To evaluate the eosinophil infiltration in lung tissues in asthmatic responses of Brown-Norway rats and guinea pigs, both of which were sensitized with ovalbumin (OA), the time course of changes in respiratory impedance (Zrs) and eosinophil influx after aerosol challenge with OA were measured. The effect of treatment with monoclonal antibody (MoAb) 1A29 against rat intercellular adhesion molecule-1 (ICAM-1) alone and a mixture of MoAb 1A29 and MoAb WT-3 against rat CD18 on asthmatic responses of the rats was studied. Finally, these expressions in lung tissues of the rats were recognized. The number of eosinophils in the subepithelial area was counted in sections of lung tissue stained with Giemsa's solution, using an Interaktive Build-Analyse System (IBAS). All of the rats and 80% of the guinea pigs developed an increase in Zrs 6-7 hours after challenge, indicating that these animals showed a late asthmatic response (LAR). The rats and the guinea pigs with a LAR had higher eosinophil counts than those with an immediate asthmatic response and sensitized, non-challenged animals (p
PubMed ID
7807750 View in PubMed
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8 records – page 1 of 1.